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Obesity Research Yields Discovery With Impact On Immunity

  December, 2 2000 3:44
your information resource in human molecular genetics
Obesity can be considered to be the result of an imbalance between energy intake and energy expenditure. The marked increase in the sedentary lifestyle in many countries is believed to contribute towards a similarly steep increase in the incidence of obesity. But even without physical exercise, the body constantly consumes energy to fuel basal metabolism. It has therefore been suggested that differences in basal energy expenditure among individuals might underlie the varying susceptibility to obesity. Cellular energy is produced by small, subcellular organelles called mitochondria; the process is made more efficient by mechanisms that ‘couple’ the different reactions involved. The discovery of the UCPs, which are able to ‘uncouple’ these reactions, indicated that they might be central to energy dissipation and led to excited speculation that higher UCP activity increases energy expenditure and concomitantly reduces fat storage.

Daniel Ricquier, of the Centre National pour la Recherche Scientifique (Meudon, France) and colleagues now show that, contrary to expectation, the weight of mice deficient in a major uncoupling protein, UCP2, is normal (Nature Genetics, Vol. 26, Issue 4, 01 Dec 2000). Noting, however, that the protein is produced by cells that mediate immunity, such as macrophages, they decided to investigate the immune response of the deficient mice. Strikingly, the mice are completely resistant to Toxoplasma gondii, a virulent parasite that infects the brains of mice and normally leads to their death. The researchers further investigated how UCP2 might ramp up macrophage activity, and found that depletion of UCP2 led to an increase in reactive oxygen species (ROS). Whereas other studies have insinuated a link between the UCPs and levels of ROS, the study by Ricquier and colleagues is the first to provide a strong correlation.

ROS, also called ‘free radicals’, are molecules with unpaired electrons, so they are extremely reactive and can cause severe cellular damage. In macrophages, high levels of ROS seem to improve immunity; bacteria or parasites engulfed by the macrophages are killed more effectively. With respect to other tissues, however, high levels of ROS are associated with morbid processes, such as rheumatoid arthritis or neurodegeneration. Therefore, the increase in ROS observed in mice lacking UCP2 is likely to be detrimental in the long run. As Antonio Vidal Puig points out in an accompanying News & Views article, the advance that the study provides in identifying a baseline control of ROS levels, and their dramatic correlation with immunity should compensate any disappointment among obesity researchers.



Dr. Daniel Ricquier, CNRS
Meudon, France
Telephone: +33 1 45 07 50 68
Fax: +33 1 45 07 58 90
E-mail: ricquier@infobiogen.fr

Dr. Sheila Collins
Duke University
Durham, North Carolina
Telephone: +1 919 684 8991
Fax: +1 919 684 3071
E-mail: colli008@mc.duke.edu

(News & Views)

Dr. Antonio Vidal-Puig
University of Cambridge
Cambridge, United Kingdom
Telephone: +44 1223 762 790
Fax: +44 1223 330 598
E-mail: ajv22@cam.ac.uk

(C) Nature Genetics press release.

Message posted by: Trevor M. D'Souza

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